Selective Nitric Oxide Synthase Inhibition Improves Microvascular Responsiveness to Endothelin-1 in Septic Mice

Broussard, Marque; Parrillo, Joseph E.; Hollenberg, Steven M.

doi:10.1097/00003246-199912001-00259

Cited by 2 publications

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“…NO overproduction due to activation by cytokine-inducible NOS has been implicated in the pathophysiology of microcirculatory failure and organ dysfunction in sepsis, and NOS inhibition was shown to prevent vasodilation and hypotension in several experimental models [ 20 - 22 ]. The nonspecific NOS inhibitor N G -methyl- L -arginine ( L -NMMA), however, did not improve mortality in a multicenter, randomized, double-blind, placebo-controlled trial of patients with septic shock, although hypotension was improved [ 23 ].…”

Section: Sepsismentioning

confidence: 99%

Bench-to-bedside review: Nitric oxide in critical illness – update 2008

Hollenberg

Cinel

2009

Crit Care

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Nitric oxide (NO) is a unique and nearly ubiquitous molecule that is widely utilized as a signaling molecule in cells throughout the body. NO is highly diffusible, labile, and multiply reactive, suiting it well for its role as an important regulator of a number of diverse biologic processes, including vascular tone and permeability, platelet adhesion, neurotransmission, and mitochondrial respiration. NO can protect cells against antioxidant injury, can inhibit leukocyte adhesion, and can participate in antimicrobial defense, but can also have deleterious effects, including inhibition of enzyme function, promotion of DNA damage, and activation of inflammatory processes. This molecule's chemistry dictates its biologic activity, which can be both direct and indirect. In addition, NO has bimodal effects in a number of cells, maintaining homeostasis at low doses, and participating in pathophysiology in others. Perturbation of NO regulation is involved in the most important and prevalent disease processes in critical care units, including sepsis, acute lung injury, and multiple organ failure. Given that NO is ubiquitous, highly diffusible, and promiscuously reactive, its regulation is complex. The NO concentration, kinetics, and localization, both inside and outside the cell, are clearly crucial factors. In the present update we review a selection of studies that have yielded important information on these complex but important issues. Interpretation of these and other studies aimed at elucidating physiologic and pathophysiologic roles of NO must take this complexity into account. A full review of the role of NO in these diseases is beyond the scope of the current manuscript; the present article will focus on recent advances in understanding the complex role of NO in health and disease.

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Section: Sepsismentioning

confidence: 99%

Bench-to-bedside review: Nitric oxide in critical illness – update 2008

Hollenberg

Cinel

2009

Crit Care

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“…In addition, it plays an important role in the response to infection [9][10][11][12] . NO synthesised in response to infection has diverse functions including bactericidal and phagocytic function by monocytes 13 and the regulation of the macro 14 and microcirculation 15,16 . The interaction between nitric oxide signalling and hypoxia is critically important in regulating the immune response to infection 17 .…”

Section: Introductionmentioning

confidence: 99%

Hypoxia causes increased monocyte nitric oxide synthesis which is mediated by changes in dimethylarginine dimethylaminohydrolase 2 expression in animal and human models of normobaric hypoxia

Lambden

Martin²,

Vanezis

et al. 2016

Nitric Oxide

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causes increased monocyte nitric oxide synthesis which is mediated by changes in dimethylarginine dimethylaminohydrolase 2 expression in animal and human models of normobaric hypoxia, Nitric Oxide (2016Oxide ( ), doi: 10.1016Oxide ( /j.niox.2016 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Background Tissue hypoxia is a cardinal feature of inflammatory diseases and modulates monocyte function. Nitric oxide is a crucial component of the immune cell response. This study explored the metabolism of the endogenous inhibitor of nitric oxide production asymmetric dimethylarginine(ADMA) by monocyte dimethylarginine dimethylaminohydrolase 2(DDAH2), and the role of this pathway in the regulation of the cellular response and the local environment during hypoxia. M A N U S C R I P T A C C E P T E D ACCEPTED MANUSCRIPT

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Selective Nitric Oxide Synthase Inhibition Improves Microvascular Responsiveness to Endothelin-1 in Septic Mice

Cited by 2 publications

References 0 publications

Bench-to-bedside review: Nitric oxide in critical illness – update 2008

Bench-to-bedside review: Nitric oxide in critical illness – update 2008

Hypoxia causes increased monocyte nitric oxide synthesis which is mediated by changes in dimethylarginine dimethylaminohydrolase 2 expression in animal and human models of normobaric hypoxia

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